Studies on the effect of environmental chemicals on cancer has primarily focused on the early stages, while the impact on later stages, particularly cancer progression, has been less explored. Cellular senescence, a response to stress such as DNA damage and oxidative stress, has been reported to play a crucial role in cancer progression. Environmental chemicals are suspected to promote cancer progression, yet it is unclear whether this is mediated through cellular senescence. Benzo[a]pyrene (BP) is known to induce DNA damage, a key trigger of senescence, but whether it directly induces senescence in cancer cells remains uncertain. This study aims to evaluate the senescence-inducing potential of BP in breast cancer cells to better understand its role in cancer progression. We examined the effects of BP, a polycyclic aromatic hydrocarbon primarily generated via incomplete combustion of organic matter and commonly found in water, soil, automobile exhaust, and tobacco smoke, on MCF7 breast cancer cells. BP enters the human body via inhalation, ingestion, and dermal contact. Here, as indicated by multiple senescence markers, including nuclear elongation, senescence-associated β-galactosidase activity, DNA damage, and increased p21 expression, BP induced cellular senescence in MCF7 cells. As cellular senescence is associated with malignant cell transformation, our results might suggest that BP contributes to cancer progression by inducing cellular senescence.